Sevoflurane preconditioning induced delayed neuroprotection against focal cerebral ischemia in rats.
- Author:
Zhi YE
1
;
Qulian GUO
;
E WANG
;
Min SHI
;
Yundan PAN
Author Information
1. Department of Anesthesia, Central South University, Changsha 410078, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Hypoxia-Ischemia, Brain;
complications;
drug therapy;
Infarction, Middle Cerebral Artery;
complications;
drug therapy;
Interleukin-1beta;
genetics;
metabolism;
Ischemic Preconditioning;
methods;
KATP Channels;
metabolism;
Male;
Methyl Ethers;
pharmacology;
therapeutic use;
Neuroprotective Agents;
pharmacology;
therapeutic use;
RNA, Messenger;
genetics;
metabolism;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Reactive Oxygen Species;
metabolism;
Reperfusion Injury;
etiology;
prevention & control;
Sevoflurane;
Tumor Necrosis Factor-alpha;
genetics;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2009;34(2):152-157
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate whether the reactive oxygen species (ROS) and mitochondrial ATP-sensitive potassium (mitoKATP) channels were involved in delayed neuroprotection induced by sevoflurane on tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) levels.
METHODS:Eighty-four male SD rats weighing 250 approximately 280 g, undergoing thread embolism of the right middle cerebral artery occlusion (MCAO) to cause focal ischemia for 2 h and then undergoing 24 h reperfusion, were randomly divided into 7 groups (n=12, each): a sham group(S), an ischemia-reperfusion group (I/R), a sevoflurane preconditioning group (Sevo), a 2-mercaptopropionylglycine (ROS scavenger)+sevoflurane group (MPG+Sevo), a 5-hydroxydecanoate (a mitoK(ATP) blocker) + sevoflurane group (5-HD+Sevo), an MPG group, and a 5-HD group. The protein level of TNF-alpha and IL-1beta in the cerebral issue was detected by enzyme linked immunosorbent assay (ELISA) and the expression of mRNA was measured by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR).
RESULTS:Apoptosis index (AI), the protein level and the mRNA expression of TNF-alpha and IL-1beta were significantly higher in the I/R group than those of Group S. Pre-administration of sevoflurane could inhibit the increase of the protein level and the expression of mRNA of TNF-alpha, and IL-1beta and attenuate the cerebral damage induced by ischemia-reperfusion. Neuroprotection of sevoflurane preconditioning was abolished by MPG and 5-HD. However, MPG and 5-HD alone had no effect.
CONCLUSION:Sevoflurane can produce delayed protection against cerebral ischemia-reperfusion injury by down-regulating TNF-alpha, IL-1beta protein, and mRNA expression.
